Evidence map›Paper›PMID 31431476›Full record

ArticleThe Journal of cell biology2019

Retromer and TBC1D5 maintain late endosomal RAB7 domains to enable amino acid-induced mTORC1 signaling.

Arunas Kvainickas, Heike Nägele, Wenjing Qi, Ladislav Dokládal, Ana Jimenez-Orgaz, Luca Stehl, Dipak Gangurde, Qian Zhao, Zehan Hu, Jörn Dengjel and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
  2. Antibody-drug conjugates in gastric cancer: clinical advances and resistance mechanisms.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026
    Review
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  6. Identification of a VPS29 isoform with restricted association to Retriever and Retromer accessory proteins through autoinhibition.Proceedings of the National Academy of Sciences of the United States of America · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 2 countries.

Arunas KvainickasCenter for Biological Systems Analysis, University of Freiburg, Freiburg, Germany.
Heike NägeleCenter for Biological Systems Analysis, University of Freiburg, Freiburg, Germany.
Wenjing QiFaculty of Biology, University of Freiburg, Freiburg, Germany.
Ladislav DokládalDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Ana Jimenez-OrgazCenter for Biological Systems Analysis, University of Freiburg, Freiburg, Germany.
Luca StehlCenter for Biological Systems Analysis, University of Freiburg, Freiburg, Germany.
Dipak GangurdeFaculty of Biology, University of Freiburg, Freiburg, Germany.
Qian ZhaoFaculty of Biology, University of Freiburg, Freiburg, Germany.ORCID 0000-0002-4017-465X
Zehan HuDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Jörn DengjelDepartment of Biology, University of Fribourg, Fribourg, Switzerland.ORCID 0000-0002-9453-4614
Claudio De VirgilioDepartment of Biology, University of Fribourg, Fribourg, Switzerland.ORCID 0000-0001-8826-4323
Ralf BaumeisterFaculty of Biology, University of Freiburg, Freiburg, Germany.
Florian SteinbergCenter for Biological Systems Analysis, University of Freiburg, Freiburg, Germany florian.steinberg@zbsa.de.ORCID 0000-0003-1849-0506
University of Freiburg · DEUniversity of Fribourg · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retromer is an evolutionarily conserved multiprotein complex that orchestrates the endocytic recycling of integral membrane proteins. Here, we demonstrate that retromer is also required to maintain lysosomal amino acid signaling through mTORC1 across species. Without retromer, amino acids no longer stimulate mTORC1 translocation to the lysosomal membrane, which leads to a loss of mTORC1 activity and increased induction of autophagy. Mechanistically, we show that its effect on mTORC1 activity is not linked to retromer's role in the recycling of transmembrane proteins. Instead, retromer cooperates with the RAB7-GAP TBC1D5 to restrict late endosomal RAB7 into microdomains that are spatially separated from the amino acid-sensing domains. Upon loss of retromer, RAB7 expands into the ragulator-decorated amino acid-sensing domains and interferes with RAG-GTPase and mTORC1 recruitment. Depletion of retromer in

Indexed as

LongevitySignal TransductionAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsMechanistic Target of Rapamycin Complex 1Membrane Microdomainsrab7 GTP-Binding Proteinsrab GTP-Binding ProteinsCaenorhabditis elegans ProteinsMechanistic Target of Rapamycin Complex 1rab7 GTP-Binding Proteinsrab GTP-Binding Proteins

Identifiers

PMID31431476
PMCPMC6719456
OpenAlexW2969230013

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.